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lüll Mediators and mechanisms of pancreatic beta-cell death in type 1 diabetes Pirot P; Cardozo AK; Eizirik DLArq Bras Endocrinol Metabol 2008[Mar]; 52 (2): 156-65Type 1 diabetes mellitus (T1D) is characterized by severe insulin deficiency resulting from chronic and progressive destruction of pancreatic beta-cells by the immune system. The triggering of autoimmunity against the beta-cells is probably caused by environmental agent(s) acting in the context of a predisposing genetic background. Once activated, the immune cells invade the islets and mediate their deleterious effects on beta-cells via mechanisms such as Fas/FasL, perforin/granzyme, reactive oxygen and nitrogen species and pro-inflammatory cytokines. Binding of cytokines to their receptors on the beta-cells activates MAP-kinases and the transcription factors STAT-1 and NFkappa-B, provoking functional impairment, endoplasmic reticulum stress and ultimately apoptosis. This review discusses the potential mediators and mechanisms leading to beta-cell destruction in T1D.|Animals[MESH]|Apoptosis/*immunology[MESH]|Autoantibodies/immunology[MESH]|Cytokines/*immunology/pharmacology[MESH]|Diabetes Mellitus, Type 1/*immunology[MESH]|Endoplasmic Reticulum/immunology/physiology[MESH]|Immune System/immunology/physiopathology[MESH]|Immunity, Cellular/immunology[MESH]|Insulin-Secreting Cells/*immunology/pathology[MESH]|Insulin/immunology/metabolism[MESH]|Major Histocompatibility Complex/genetics[MESH]|Mice[MESH]|Mice, Inbred NOD[MESH]|Polymorphism, Genetic[MESH] |